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| http://dx.doi.org/10.1016/j.yjmcc.2025.08.007 | DOI Listing |
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Response to: Cytoplasmic RBM20 gain-of-function induces atrial arrhythmogenicity independent of splicing defects in a novel murine model by Brijesh Sathian et al.
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Cytoplasmic mutant RBM20 causes arrhythmogenicity in murine atria.
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RNA binding motif protein 20 (RBM20) is a critical splicing regulator in cardiomyocytes, and mutations in its RSRSP domain are associated with severe dilated cardiomyopathy (DCM) and a high prevalence of atrial fibrillation (AF). RBM20 mutation has long been thought to cause DCM through the disturbed splicing of the target genes by its loss of function. However, recent studies have highlighted that the gain of function of mutant RBM20, independent of splicing defects, may also play a critical role in the pathogenesis of DCM.
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Department of Animal and Dairy Sciences, (Y.Z., Z.R.G., Y.H., C.L., W.G.), University of Wisconsin-Madison.
Background: RBM20 (RNA binding motif protein 20) cardiomyopathy is a severe form of dilated cardiomyopathy (DCM). Genetic variants in the nuclear localization signal of hinder its nuclear import and promote cytoplasmic pathogenic RNP (ribonucleoprotein) granules. We aimed to investigate whether reducing RNP granules by inhibiting expression could alleviate the DCM phenotype in S639G () knock-in mice.
View Article and Find Full Text PDFAntisense-mediated regulation of exon usage in the elastic spring region of Titin modulates sarcomere function.
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Division of Cardiology, Department of Clinical Sciences, Lund University, BMC D12, Solvegatan 19, Lund SE-221 84, Sweden.
Aims: Alternative splicing of Titin (TTN) I-band exons produce protein isoforms with variable size and elasticity, but the mechanisms whereby TTN splice factors regulate exon usage and thereby determining cardiomyocyte passive stiffness and diastolic function, is not well understood. Non-coding RNA transcripts from the antisense strand of protein-coding genes have been shown to regulate alternative splicing of the sense gene. The TTN gene locus harbours >80 natural antisense transcripts (NATs) with unknown function in the human heart.
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